Component
Kynurenic acid
Independently recorded entity or measured process. Linked claims specify compartment, assay and experimental scope.
11 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
Mouse hippocampal alpha7 currents remained insensitive to kynurenic acid, including slices prepared and stored in 1 mM for over 90 minutes, although glutamatergic currents were blocked.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse hilar and stratum-radiatum interneuron recordings.
- limitations
- Does not mean kynurenic acid has no neural effects.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- The negative receptor result persisted with prolonged high exposure and a positive pharmacological control.
- primary_references
- Lack of modulation of nicotinic acetylcholine alpha-7 receptor currents by kynurenic acid in adult hippocampal interneurons. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22848433/ · DOI 10.1371/journal.pone.0041108
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 306–312
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse hilar and stratum-radiatum interneuron recordings. · source_derived_draft · unverified_draft
## tryptophan-kyna-alpha7-mouse-null The negative receptor result persisted with prolonged high exposure and a positive pharmacological control. Mouse hippocampal alpha7 currents remained insensitive to kynurenic acid, including slices prepared and stored in 1 mM for over 90 minutes, although glutamatergic currents were blocked. Model: Mouse hilar and stratum-radiatum interneuron recordings. Limitations: Does not mean kynurenic acid has no neural effects. Evidence access: Primary abstract Lack of modulation of nicotinic acetylcholine alpha-7 receptor currents by kynurenic acid in adult hippocampal interneurons. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22848433/ · DOI 10.1371/journal.pone.0041108
Complete structured claim and evidenceKynurenic acid inhibited alpha7 nicotinic responses in cultured rat hippocampal neurons after at least four minutes, with an IC50 near 7 micromolar.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Rat hippocampal culture and slice electrophysiology.
- limitations
- Direct alpha7 inhibition is disputed by a later slice study; retain assay context rather than treating it as universal.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- One laboratory reported suppression of an acetylcholine receptor.
- primary_references
- The brain metabolite kynurenic acid inhibits alpha7 nicotinic receptor activity and increases non-alpha7 nicotinic receptor expression: physiopathological implications. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11567036/ · DOI 10.1523/JNEUROSCI.21-19-07463.2001
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat hippocampal culture and slice electrophysiology. · source_derived_draft · unverified_draft
## tryptophan-kyna-alpha7-positive One laboratory reported suppression of an acetylcholine receptor. Kynurenic acid inhibited alpha7 nicotinic responses in cultured rat hippocampal neurons after at least four minutes, with an IC50 near 7 micromolar. Model: Rat hippocampal culture and slice electrophysiology. Limitations: Direct alpha7 inhibition is disputed by a later slice study; retain assay context rather than treating it as universal. Evidence access: Primary abstract The brain metabolite kynurenic acid inhibits alpha7 nicotinic receptor activity and increases non-alpha7 nicotinic receptor expression: physiopathological implications. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11567036/ · DOI 10.1523/JNEUROSCI.21-19-07463.2001
Complete structured claim and evidenceKynurenic acid did not inhibit choline-evoked alpha7 currents in rat hippocampal slice interneurons, contrasting with earlier reports.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Adolescent rat stratum-radiatum interneurons in acute slices.
- limitations
- Slice age, temperature, agonist delivery and receptor environment are candidate explanations, not a demonstrated resolution.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Another experiment did not reproduce the claimed receptor block.
- primary_references
- Lack of modulation of nicotinic acetylcholine alpha-7 receptor currents by kynurenic acid in adult hippocampal interneurons. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22848433/ · DOI 10.1371/journal.pone.0041108
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 298–304
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Adolescent rat stratum-radiatum interneurons in acute slices. · source_derived_draft · unverified_draft
## tryptophan-kyna-alpha7-rat-null Another experiment did not reproduce the claimed receptor block. Kynurenic acid did not inhibit choline-evoked alpha7 currents in rat hippocampal slice interneurons, contrasting with earlier reports. Model: Adolescent rat stratum-radiatum interneurons in acute slices. Limitations: Slice age, temperature, agonist delivery and receptor environment are candidate explanations, not a demonstrated resolution. Evidence access: Primary abstract Lack of modulation of nicotinic acetylcholine alpha-7 receptor currents by kynurenic acid in adult hippocampal interneurons. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22848433/ · DOI 10.1371/journal.pone.0041108
Complete structured claim and evidence
What acts on it
Human KAT-II transaminates kynurenine to an intermediate that leads to kynurenic acid.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human enzyme structural study and catalytic characterization.
- limitations
- The enzyme performs transamination; it does not directly perform every subsequent chemical rearrangement.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Kynurenine can be diverted into a neuroactive branch.
- primary_references
- Structure of the PLP-Form of the Human Kynurenine Aminotransferase II in a Novel Spacegroup at 1.83 Å Resolution. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27023527/ · DOI 10.3390/ijms17040446
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 210–216
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human enzyme structural study and catalytic characterization. · source_derived_draft · unverified_draft
## tryptophan-kat2-kyna Kynurenine can be diverted into a neuroactive branch. Human KAT-II transaminates kynurenine to an intermediate that leads to kynurenic acid. Model: Human enzyme structural study and catalytic characterization. Limitations: The enzyme performs transamination; it does not directly perform every subsequent chemical rearrangement. Evidence access: Primary abstract Structure of the PLP-Form of the Human Kynurenine Aminotransferase II in a Novel Spacegroup at 1.83 Å Resolution. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27023527/ · DOI 10.3390/ijms17040446
Complete structured claim and evidence
Where it participates (unsigned role)
3-Hydroxykynurenine increased 39% fasting and 34% after meals; kynurenic acid decreased 22% and 20%, respectively.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- B6-dependent kynurenine reactions intersect the tryptophan-to-niacin network; conversion to NAD was not measured.
- experimental_model
- Twenty-three healthy adults; paired pre/postprandial LC-MS/MS metabolite profiling.
- exposure
- 28 days below 0.35 mg/day B6. Related restriction research program; do not count paper totals as independent trial replications.
- limitations
- Does not measure brain neurotransmitters, tissue NAD synthesis or diagnose niacin deficiency.
- nutrient_topic
- Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
- organism
- Homo sapiens
- plain_language
- Different branches of tryptophan processing left a detectable blood pattern.
- primary_references
- [b6-dasilva2013] Metabolite profile analysis reveals functional effects of 28-day vitamin B-6 restriction on one-carbon metabolism and tryptophan catabolic pathways in healthy men and women (2013). https://pubmed.ncbi.nlm.nih.gov/23966327/ DOI: 10.3945/jn.113.180588
- tissue_or_cell_type
- Human blood and whole-body measurements
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1436–1447
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twenty-three healthy adults; paired pre/postprandial LC-MS/MS metabolite profiling. · source_derived_draft · unverified_draft
### b6-restriction-kynurenine-profile 3-Hydroxykynurenine increased 39% fasting and 34% after meals; kynurenic acid decreased 22% and 20%, respectively. Condition category: nutrient_deficiency nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different branches of tryptophan processing left a detectable blood pattern. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Twenty-three healthy adults; paired pre/postprandial LC-MS/MS metabolite profiling. limitations: Does not measure brain neurotransmitters, tissue NAD synthesis or diagnose niacin deficiency. exposure: 28 days below 0.35 mg/day B6. Related restriction research program; do not count paper totals as independent trial replications. cross_nutrient: B6-dependent kynurenine reactions intersect the tryptophan-to-niacin network; conversion to NAD was not measured. [b6-dasilva2013] Metabolite profile analysis reveals functional effects of 28-day vitamin B-6 restriction on one-carbon metabolism and tryptophan catabolic pathways in healthy men and women (2013). https://pubmed.ncbi.nlm.nih.gov/23966327/ DOI: 10.3945/jn.113.180588
Complete structured claim and evidenceKynurenic-acid NMDA-blocking IC50 shifted from about 15 to 235 micromolar when 10 micromolar glycine was present.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Rat neuronal electrophysiological assay.
- limitations
- An assay co-agonist effect does not show that glycine supplements change human disease outcomes.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- A second amino acid changed how strongly the metabolite blocked a receptor.
- primary_references
- The brain metabolite kynurenic acid inhibits alpha7 nicotinic receptor activity and increases non-alpha7 nicotinic receptor expression: physiopathological implications. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11567036/ · DOI 10.1523/JNEUROSCI.21-19-07463.2001
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 314–320
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat neuronal electrophysiological assay. · source_derived_draft · unverified_draft
## tryptophan-glycine-kyna-nmda A second amino acid changed how strongly the metabolite blocked a receptor. Kynurenic-acid NMDA-blocking IC50 shifted from about 15 to 235 micromolar when 10 micromolar glycine was present. Model: Rat neuronal electrophysiological assay. Limitations: An assay co-agonist effect does not show that glycine supplements change human disease outcomes. Evidence access: Primary abstract The brain metabolite kynurenic acid inhibits alpha7 nicotinic receptor activity and increases non-alpha7 nicotinic receptor expression: physiopathological implications. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11567036/ · DOI 10.1523/JNEUROSCI.21-19-07463.2001
Complete structured claim and evidenceIL4I1 generated indole metabolites and kynurenic acid that activated AHR in the cancer study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human cancer/biochemical work with separate mouse CLL experiments.
- limitations
- This abstract groups several products; their individual concentrations and relative causal contributions are not resolved here.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Another enzyme can feed the same receptor through different metabolites.
- primary_references
- IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32818467/ · DOI 10.1016/j.cell.2020.07.038
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human cancer/biochemical work with separate mouse CLL experiments. · source_derived_draft · unverified_draft
## tryptophan-il4i1-route Another enzyme can feed the same receptor through different metabolites. IL4I1 generated indole metabolites and kynurenic acid that activated AHR in the cancer study. Model: Human cancer/biochemical work with separate mouse CLL experiments. Limitations: This abstract groups several products; their individual concentrations and relative causal contributions are not resolved here. Evidence access: Primary abstract IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32818467/ · DOI 10.1016/j.cell.2020.07.038
Complete structured claim and evidenceHuman KAT-II/AADAT is a PLP-dependent homodimer; the structure shows a PLP–Lys263 aldimine at its catalytic site.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human KAT-II crystal structure at 1.83 angstrom resolution.
- limitations
- Cofactor dependence alone does not define clinical B6 requirements or benefit from excess B6.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Vitamin B6 participates in a branch enzyme, not only the serotonin route.
- primary_references
- Structure of the PLP-Form of the Human Kynurenine Aminotransferase II in a Novel Spacegroup at 1.83 Å Resolution. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27023527/ · DOI 10.3390/ijms17040446
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 202–208
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human KAT-II crystal structure at 1.83 angstrom resolution. · source_derived_draft · unverified_draft
## tryptophan-kat2-plp Vitamin B6 participates in a branch enzyme, not only the serotonin route. Human KAT-II/AADAT is a PLP-dependent homodimer; the structure shows a PLP–Lys263 aldimine at its catalytic site. Model: Human KAT-II crystal structure at 1.83 angstrom resolution. Limitations: Cofactor dependence alone does not define clinical B6 requirements or benefit from excess B6. Evidence access: Primary abstract Structure of the PLP-Form of the Human Kynurenine Aminotransferase II in a Novel Spacegroup at 1.83 Å Resolution. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27023527/ · DOI 10.3390/ijms17040446
Complete structured claim and evidenceMuscle-specific PGC-1alpha1 transgenic mice resisted depression-like changes induced by chronic mild stress or kynurenine administration as peripheral kynurenine handling shifted.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse genetic overexpression and behavioral challenges.
- limitations
- Not proof that this is the sole human exercise–mood mechanism or that kynurenic acid freely enters the brain.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- A peripheral metabolic change altered a brain-related behavioral response.
- primary_references
- Skeletal muscle PGC-1α1 modulates kynurenine metabolism and mediates resilience to stress-induced depression. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25259918/ · DOI 10.1016/j.cell.2014.07.051
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 618–624
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic overexpression and behavioral challenges. · source_derived_draft · unverified_draft
## tryptophan-muscle-brain-context A peripheral metabolic change altered a brain-related behavioral response. Muscle-specific PGC-1alpha1 transgenic mice resisted depression-like changes induced by chronic mild stress or kynurenine administration as peripheral kynurenine handling shifted. Model: Mouse genetic overexpression and behavioral challenges. Limitations: Not proof that this is the sole human exercise–mood mechanism or that kynurenic acid freely enters the brain. Evidence access: Primary abstract Skeletal muscle PGC-1α1 modulates kynurenine metabolism and mediates resilience to stress-induced depression. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25259918/ · DOI 10.1016/j.cell.2014.07.051
Complete structured claim and evidenceCarbidopa inhibition of kynurenine aminotransferase activity impaired aspartate synthesis and mitochondrial respiration and reduced mouse exercise performance and muscle force.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mouse muscle/exercise experiments within a PGC-1alpha1 and malate–aspartate-shuttle study.
- limitations
- Carbidopa is not specific to a single KAT isoform; mouse exposures do not establish the same effect at a clinical human dose.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- The branch can support muscle energy handling as well as alter circulating metabolites.
- primary_references
- Skeletal muscle PGC-1α1 reroutes kynurenine metabolism to increase energy efficiency and fatigue-resistance. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31235694/ · DOI 10.1038/s41467-019-10712-0
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 626–632
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse muscle/exercise experiments within a PGC-1alpha1 and malate–aspartate-shuttle study. · source_derived_draft · unverified_draft
## tryptophan-muscle-kat-inhibition The branch can support muscle energy handling as well as alter circulating metabolites. Carbidopa inhibition of kynurenine aminotransferase activity impaired aspartate synthesis and mitochondrial respiration and reduced mouse exercise performance and muscle force. Model: Mouse muscle/exercise experiments within a PGC-1alpha1 and malate–aspartate-shuttle study. Limitations: Carbidopa is not specific to a single KAT isoform; mouse exposures do not establish the same effect at a clinical human dose. Evidence access: Primary abstract Skeletal muscle PGC-1α1 reroutes kynurenine metabolism to increase energy efficiency and fatigue-resistance. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31235694/ · DOI 10.1038/s41467-019-10712-0
Complete structured claim and evidenceThe PGC-1alpha1–PPAR-alpha/delta program increased muscle kynurenine aminotransferases and conversion of kynurenine to kynurenic acid.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse skeletal-muscle transgenic and stress experiments.
- limitations
- Multiple aminotransferases are involved; do not assign the entire effect to human AADAT alone.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Muscle metabolism can change which tryptophan products remain in circulation.
- primary_references
- Skeletal muscle PGC-1α1 modulates kynurenine metabolism and mediates resilience to stress-induced depression. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25259918/ · DOI 10.1016/j.cell.2014.07.051
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 610–616
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse skeletal-muscle transgenic and stress experiments. · source_derived_draft · unverified_draft
## tryptophan-muscle-kat-program Muscle metabolism can change which tryptophan products remain in circulation. The PGC-1alpha1–PPAR-alpha/delta program increased muscle kynurenine aminotransferases and conversion of kynurenine to kynurenic acid. Model: Mouse skeletal-muscle transgenic and stress experiments. Limitations: Multiple aminotransferases are involved; do not assign the entire effect to human AADAT alone. Evidence access: Primary abstract Skeletal muscle PGC-1α1 modulates kynurenine metabolism and mediates resilience to stress-induced depression. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25259918/ · DOI 10.1016/j.cell.2014.07.051
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.